The Pulmonary Artery Lasso: Epicardial Pacing Lead Causing Right Ventricular Outflow Obstruction

Permanent pacing in small children may require placement of an epicardial pacing system. This report describes a young child who underwent pacemaker implantation with epicardial ventricular lead placement in infancy as an adjunct to antiarrhythmic therapy for congenital junctional ectopic tachycardia. At 5 years of age, a harsh systolic murmur was detected for the first time. Evaluation by catheterization and transluminal echocardiography showed right ventricular outflow obstruction (pressure gradient 40 mmHg) secondary to extrinsic compression by the epicardial lead. Surgical removal of the lead relieved the obstruction.     

Unusual pacing observed in a biventricular pacemaker with epicardial pacing leads

In this case report, we describe inappropriate pacing in a patient with a newly implanted biventricular pacing system with three epicardial leads. Very high pacing thresholds resulted from the use of nonsteroid eluting leads, and unusual pacing behavior was due to the chosen implant locations for the right atrial and right ventricular epicardial leads. The interplay between the programmed pacemaker parameters, the very late ventricular sensing in the setting of intrinsic right bundle branch block, and atrial lead oversensing led to ineffective biventricular pacing. The persistently elevated pacing thresholds and sensing problems led to very early battery depletion and the need to replace the epicardial system with three new endocardial leads.     

Ventricular Pacing Threshold and Time to Capture Postdefibrillation in Patients Undergoing Implantable Cardioverter-Defibrillator Implantation

To assess the effect of defibrillation and amiodarone on ventricular pacing threshold and time to capture in patients undergoing automatic implantable cardioverter-defibrillator (AICD) implantation, 28 patients were prospectively evaluated. The patients were entered into one of two protocols: la—epicardial ventricular pacing threshold measured at baseline (preventricular fibrillation induction) and 10 and 60 seconds postdefibrillation with 20 J, or Ib—two fibrillation-defibrillation sequences were performed 3 minutes apart and ventricular pacing thresholds were measured for each sequence at baseline and at 10 and 60 seconds postdefibrillation with 20 J. Ten patients also underwent asynchronous pacing at 1.1 times baseline threshold during ventricular fibrillation with measurement of time to capture postdefibrillation. All patients were randomly assigned to receive either amiodarone or no antiarrhythmic drug therapy. Ventricular fibrillation was induced with AC (applied for 1-2 seconds), and standard epicardial bipolar and epicardial patch electrodes of the AICD were used for pacing and defibrillation, respectively. Ventricular pacing threshold at baseline, 10 seconds, 60 seconds, and 3 minutes postdefibrillation did not differ significantly. There were no significant differences in patients with or without amiodarone therapy. Furthermore, there was no transient loss of ventricular capture postdefibrillation or significant difference in time to capture with amiodarone (≤ 2 seconds). We conclude that following internal defibrillation with 20 J: (1) ventricular pacing threshold at 10 seconds, 60 seconds, and 3 minutes were not significantly different from baseline with one or two fibrillation-defibrillation sequences, (2) time to capture was short, and (3) there was no significant difference in no drug versus amiodarone. These findings have direct clinical importance in considering device therapy with both pacing and defibrillating capabilities.     

Increased Pacing Threshold After an Automatic Defibrillator Shock in Dogs: Effects of Class I and Class II Antiarrhythmic Drugs

A high energy shock delivered by an automatic defibrillator may interfere with pacemaker function. To provide insight into the changes that occur in the threshold for ventricular pacing after the shock from an automatic defibrillator, we measured the time to capture during asynchronous ventricular pacing in dogs from endocardial or epicardial sites, after a 30 joule shock was delivered via conventional automatic defibrillator (AICD) patch electrodes. After a 30 joule shock, there was a transient loss of ventricular capture. The duration of capture loss was related to current strength. During endocardial pacing at threshold current, the time to capture was 4.9 +/- 1.2 s, whereas at current values twice threshold the time to capture from endocardial pacing was 2.2 +/- 0.9 s. No difference was found between endocardial and epicardial pacing sites in the time to capture. To ascertain the mechanism of capture loss we: (1) examined the effects of converting the pacing catheter to a current sink (transiently shunting to ground); (2) altered excitability by an infusion of flecainide; (3) blocked sympathetic input (propranolol). No change in time to capture was noted by shunting the pacer to ground. After an infusion of flecainide the time to capture from endocardial pacing was significantly prolonged to 14.9 +/- 2.2 s at the threshold value (P less than .01) and 5.6 +/- 2.1 s at twice threshold (P less than .05). Conversely, intravenous propranolol had no effect on the time to capture after shock from endocardial pacing. These data indicate that there is a transient increase in pacing threshold after the shock from an automatic defibrillator.(ABSTRACT TRUNCATED AT 250 WORDS)     

Acute and Chronic Cycle Length Dependent Increase in Ventricular Pacing Threshold

Several factors have been shown to influence ventricuJar pacing threshold in humans, including pacing lead location (endocardial vs epicardial), lead maturation, and antiarrhythmic agents. To determine whether ventricuJar pacing rate has a significant influence on acute and chronic pacing thresholds, we measured pacing thresholds in 16 patients receiving an implantafaleantitachycardia pacemaker cardioverter defibrillator (Cadence?). Ventricular pacing thresholds were determined using the device programmer at cycle lengths of GOO, 400, and 300 msec at the time of implantation; prior to hospital discharge at 3-14 days; and during follow-up outpatient visits at 6-8 weeks, 3 months, and 6 months to 1 year. Eleven patients had an epicardial lead system and five an endocardial lead system. Eleven patients were being treated with antiarrhythmic drug therapy. Device output ranged from 1-10 V and was adjustable in 1-V increments (pulse width was held constant at 1 msec). A cycle length dependent increase in pacing threshold (defined as a ≤ 1-V increase in threshold at 400 or 300 msec relative to 600 msecj was observed in 10/16 patients during 12/72 pacing trials at 400 msec, and in 15/16 patients during 31/67 trials at 300 msec. In trials in which an increase in pacing threshold occurred, the magnitude of the increase at 400 msec relative to 600 msec was only 1 V in all 12 trials, but at 300 msec the increase ranged from 4–9 V in 7/31 (23%) trials. There was an equal percentage (67%) of patients demonstrating a cycle length dependent increase in threshold with measurements made at the time of device implantation and at the 6 month to 1 year follow-up period. Two-way analysis of variance showed a significant effect of cycle length and time from implantation on mean pacing thresholds at the three cycle lengths. In conclusion, a cycle length dependent increase in pacing threshold occurred in virtually all patients during follow-up of up to 12 months and, thus, its presence was independent of lead location, presence of antiarrhythmic agents, and the state of lead maturation. These findings suggest that pacing thresholds measured at rates just above the sinus rate may not always apply to the faster rates utilized for antitachycardia pacing and indicates the need for threshold measurement at the designed pacing rate.     

The Use of Left Ventricular Epicardial Surface Velocity Patterns as a Marker of Pacing Site

Ectopic ventricular foci were simulated at selected endocardial sites in 15 closed-chest canines using ventricular pacing. During this pacing, a noninvasive x-ray backscatter imaging technique was used to measure epicardial LV displacements at 5-ms intervals during the cardiac cycle. These displacement measurements were used to calculate epicardial surface velocities in each study and were presented as a time sequence of color coded velocity maps. Characteristic patterns in the timing and spatial propagation of LV surface velocities were noted for each pacing site, particularly during the expansion of the LV during isovolumic contraction and the inward motion of the LV during ejection. Average surface velocity maps for the 15 canines were computed for each pacing site. These average maps were used as standards for comparison with individual pacing studies to determine the probable site of pacing. Comparisons were made using a computer algorithm, based upon auto- and cross-correlation techniques in the time domain. This algorithm correctly identified pacing sites with sensitivities of HA 74%, LV 76%, RV 79%, and RVOT 77% and specificities of RA 98%, LV 96%, RV 90%, and RVOT 93%. The results show that this noninvasive mapping procedure has potential for identifying the location of an ectopic ventricular focus.     

Automatic ventricular threshold measurement in children with epicardial pacing leads

BACKGROUND: The aim of the study was to evaluate the safety and reliability of automatic ventricular pacing threshold measurement, the Medtronic Capture Management (CM), in children with epicardial pacing leads. CM has not been recommended for use with epicardial leads due to lack of pertinent data. METHODS: During a 2-year study period, 34 children (mean age 6.1 years, range 0 days to 17.7 years) with epicardial leads were prospectively enrolled. The CM measurements were compared with in-office ventricular pacing threshold measurements. Thirty bipolar and five unipolar epicardial leads were assessed. RESULTS: CM measurements were successful and reliable in 30 out of 35 leads (86%). The mean threshold with CM was 1.16 V (95% CI 1.07-1.26 V), and with standard measurement was 1.18 V (95% CI 1.09-1.28 V), at a pulse width of 0.40 ms. The reasons for failure were evoked response undersensing in two cases (5.7%), and high intrinsic rate in one case. High pacing thresholds prevented accurate CM measurements in two cases. CONCLUSIONS: CM automatic threshold measurements are consistent with standard ventricular pacing threshold measurements in children with epicardial leads. We recommend a period of monitoring CM performance before programming it to adjust output according to automatic threshold measurements, in order to find the patients in whom it does not work. The CM feature provides increased pacing safety when it measures well (86% of leads). A larger study is needed to prove the tendency for extending battery life in children with epicardial leads.     

Origin of electrical activation within the right atrial and left ventricular walls: differentiation by electrogram characteristics using the noncontact mapping system

Clinical data using the noncontact mapping system (Ensite 3000) suggest that characteristics of the reconstructed unipolar electrograms may predict the origin of electrical activation within the atrial and ventricular walls (endocardial vs myocardial vs epicardial origin). Experimental data are lacking. In ten open-chest pigs (mean body weight 62 kg) cardiac pacing was performed at a cycle length of 600 ms with a pulse width of 2 ms and twice diastolic threshold from the endo-, the myo-, and the epicardium, respectively. Pacing was undertaken at three right atrial and three left ventricular sites, and cardiac activation was recorded with the Ensite system. Reconstructed unipolar electrograms at the location of earliest endocardial activation assessed by color coded isopotential maps were analyzed systematically for differences in morphology. The positive predictive value of atrial electrograms exhibiting an initial R wave during pacing for a subendocardial origin (i.e., myocardial or epicardial) was 0.96. The negative predictive value was 0.48. Electrograms generated during myocardial pacing exhibited increased maximal negative voltage and maximal dV/dt (-3 +/- 1.8 mV, -798 +/- 860 mV/ms, respectively) than the electrograms obtained during endocardial (-2 +/- 1 mV, -377 +/- 251 mV/ms, respectively) and epicardial pacing (-2.1 +/- 0.7 mV, -440 +/- 401 mV/ms, respectively, P<0.01 for both parameters). During pacing at the left ventricular wall, occurrence of an initial R wave did not differ significantly between electrograms reconstructed during endocardial and subendocardial pacing. All other characteristics of the unipolar ventricular electrograms analyzed, except latency, did not differ significantly when compared to stimulation depth. Morphological characteristics of unipolar electrograms generated by the noncontact mapping system during pacing of the atrium allowed for discrimination of an endocardial versus a subendocardial origin of activation. At the ventricular level, characteristics of unipolar electrograms did not predict the origin of cardiac activation in this experimental setting.     

A New Low Threshold Platinized Epicardial Pacing Electrode: Comparative Evaluation in Immature Canines

A prospective comparison of pacing and sensing capabilities between the conventional Medtronic Model 4951 platinum-iridium epicardial pacing electrode and a new modified "platinized" version of the same electrode was performed in immature canines to determine if the new electrode design improves pacing in the immature myocardium. The conventional electrode was modified by electroplating platinum black particles onto the surface to increase the effective or true microscopic surface area, yet essentially maintain the same overall geometric electrode size. Both epicardial electrodes were inserted into the right ventricular myocardium with the lead pad sutured to the epicardium, and externalized to the scruff in five puppies (age 3 months). An additional left ventricular lead was implanted to permit chronic pacing following epicardially-induced atrioventricular block. Acute and chronic sensing and pacing capabilities of each externalized electrode were performed at implant and weekly up to 4 months. Histologic examination of each electrode implant site was performed at the end of the study period. At implant, both electrodes exhibited comparable values for sensed R waves, lead impedances, and pacing thresholds. During the study, the platinized electrode exhibited lower pacing thresholds. Analysis of all postimplant data demonstrated this threshold difference to be significantly lower (P less than .01) for the platinized version. Lead impedance and sensing capabilities remained comparable between the two designs. Histologic study demonstrated less fibrotic infiltration at the platinized electrode site. This preliminary evaluation indicates that for the duration of the postimplant study period, the platinized epicardial electrode design was associated with significantly lower thresholds and less fibrosis as a function of time compared to the conventional smooth electrode surface design. The new platinized electrode limits exit block in the developing immature myocardium and permits safe pacing at lower pulse widths and voltages to increase battery life.     

Effects of proximal ventricular septal pacing on hemodynamics and ventricular activation

Recently the use of alternate site pacing to improve cardiac function in patients with bradyarrhythmias has increased. In the present study, hemodynamics of right ventricular septal pacing were studied in seven dogs. A bipolar screw-in lead and endocardial lead were placed in the proximal right ventricular septum and right ventricular apex, respectively. The right ventricle was paced from each site. A conductance catheter and Millar catheter were inserted into the left ventricle to determine the left ventricular pressure and the pressure-volume loop. Cardiac output was measured using the thermodilution method. In five of the seven dogs, ventricular activation was documented by isochronal epicardial activation mapping during each pacing mode. Mean arterial pressure and cardiac output during septal pacing were significantly higher than during apical pacing (110 +/- 17 mmHg vs 100 +/- 18 mmHg; 1.00 +/- 0.39 L/min vs 0.89 +/- 0.33 L/min). The positive dp/dt during septal pacing was significantly higher than during apical pacing (2137 +/- 535 mmHg/s vs 1911 +/- 404 mmHg/s). End-systolic elastance during septal pacing was significantly higher compared to apical pacing (13.1 +/- 0.3 mmHg/mL vs 8.9 +/- 4.0 mmHg/mL). The ventricular activation time during septal pacing was significantly shorter than during apical pacing. The epicardial maps generated during septal pacing were similar to those from atrial pacing. We conclude that hemodynamics and interventricular conduction are less disturbed by proximal right ventricular septal pacing than apical pacing in dogs with normal hearts.     

Ventricular pacing threshold variations in the young

Ventricular Capture Management (VCM) is a Medtronic Kappa pacemakers (PM) feature that automatically measures pacing threshold through detection of the evoked response after a pacing stimulus. The aim of this study was to evaluate the range of variation of ventricular pacing threshold in pediatric patients with endocardial and epicardial pacing leads. Thirty-one patients (median age 6.5 years) were implanted with a Kappa 901 PM for atrioventricular block or sinus node dysfunction. Congenital heart defects (CHD) were present in 58% of patients. Ventricular leads were epicardial in 52% of patients. VCM was programmed to automatically measure threshold every 2 hours. In a median follow-up of 12 months, 27,110 threshold measurements, 72% of which were successful, have been taken in 94% of patients. Measurement success was 99% in the endocardial leads group (age at implantation 12 +/- 6 years) and 31% in epicardial leads (age 4 +/- 5 years) (P < 0.05). Main reasons for unsuccessful measurements were high heart rate and, in a patient with an endocardial lead, competition with intrinsic rhythm. Undersensing or oversensing of the evoked responses was not detected. In all successful VCM measurements, epicardial pacing and CHD contributed to stability of thresholds (multivariate analysis). Pacing threshold showed specific circadian patterns: higher thresholds were found between 00.00 and 06.00 a.m., but the variation was low, 0.03 +/- 0.01 V. In conclusion, children and young patients show stable ventricular thresholds, especially in presence of CHD, and epicardial leads are at least as stable as endocardial leads. Ventricular pacing threshold showed a circadian variability similar to that described in adults, that does not seem to influence VCM functioning and PM programming.     

Late Purulent Pacemaker Pocket Infection Caused by Staphylococcus Epidermidis: Serious Complications of In Situ Management

The pathophysiology of late pacemaker pocket infection is poorly understood. We report three cases of late infection caused by Staphylococcus epidermidis. Despite initial local conservative management ultimate removal of the entire pacing system was required. In late pacemaker pocket infection we recommend initial removal of the entire pacing system and replacement on the contralateral side. When retrieval of the lead system requires open-heart surgery epicardial wires should be placed.     

Maintenance of AV synchrony in a small child utilizing two pacemakers and the triggered VVT mode: triggered pacing in small children

Infants and small children with atrioventricular (AV) nodal disease frequently require pacing in order to maintain an adequate heart rate. The maintenance of AV synchrony is physiologically optimal in this setting. Unfortunately, small size and congenital anomalies often preclude the placement of standard transvenous dual chamber pacing systems. We report the case of a small child with a pre-existing dual chamber epicardial pacing system and subsequent ventricular lead dysfunction who underwent implantation of a new single chamber transvenous system which was programmed in VVT (triggered) mode in order to maintain AV synchrony.     

Rectus Abdominis as a Source of Myopotentials Inhibiting Demand Pacemakers

We examined four patients with a demand pacemaker who exhibited transient symptoms of vertigo while trying to rise from the supine position. In two of these there was an epicardial pacing system with the pacemaker in the abdominal wall superficial to the rectus abdominis muscle; in the other two cases the pacing system was transvenous with the pacemaker superficial to the right pectoralis major muscle. It was found that the "pseudovertigo" was due to pacemaker inhibition caused by rectus abdominis myopotentials in all four patients. Changing the pacing mode from demand to fixed-rate resulted in the disappearance of all symptoms at rest and during exercise.     

Achieving Permanent Left Ventricular Pacing—Options and Choice

Cardiac resynchronization therapy (CRT) requires permanent left ventricular (LV) pacing. Coronary sinus (CS) lead placement is the first line clinical approach but can be difficult or impossible; may suffer from a high LV pacing threshold, phrenic nerve stimulation, and dislodgement; and produces epicardial LV pacing, which is less physiological and hemodynamically effective and potentially more proarrhythmic than endocardial LV pacing. CS leads can usually be extracted with direct traction but may require use of extraction sheaths. Half of CS side branches previously used for lead placement may be unusable for the same purpose after successful lead extraction, and 30% of CS lead reimplantation attempts may fail due to exhaustion of side branches. Surgical epicardial LV lead placement is the more invasive second line approach, produces epicardial LV pacing, and has a lead failure rate of ≈15% in 5 years. Transseptal endocardial LV lead placement is the third line approach, can be difficult to achieve, but produces endocardial LV pacing. The major concern with transseptal endocardial LV leads is systemic thromboembolism, but the risk is unknown and oral anticoagulation is advised. Among the new CRT recipients in the United States and Western Europe between 2003 and 2007, 22,798 patients may require CS lead revisions, 9,119 patients may have no usable side branches for CS lead replacement, and 1,800 patients may require surgical epicardial LV lead revision in the next 5 years. The CRT community should actively explore and develop alternative approaches to LV pacing to meet this anticipated clinical demand.     

Steroid-Eluting Epicardial Pacing Electrodes: Six Year Experience of Pacing Thresholds in a Growing Pediatric Population

Indications for pacemaker implantation in the pediatric population often include sinus or atrioventricular node dysfunction following surgery for congenital heart defects. However, patient size, cardiac defects, and vascular and valvular concerns may limit transvenous lead utilization. Since the epicardial surface of these patients often exhibits variable degrees of fibrosis from scar tissue formation or pericardial adhesions, chronic low output (2.5/1.6 V, 0.3 ms) epicardial pacing from implant is not currently recommended in children due to frequent threshold changes and electrode exit block. As a result, pacing in children is often viewed as a less efficient system than in adults. The addition of steroid combined with newer low threshold electrode designs however stabilizes the electrode-tissue interface and eliminates postimplant changes seen with standard smooth surface electrodes potentially permitting efficient chronic pacemaker application to all patient ages. The stability of chronic low output epicardial pacing with steroid-eluting electrodes was prospectively studied in 22 patients (ages 2 days-18.5 years, median 3.5 years) for up to 6 years. Chronic pulse width thresholds were compared according to implant site and association of prior cardiac surgery. A total of 26 pacing leads were implanted. The acute implant mean pulse width threshold (2.5 V) for all the electrodes studied was 0.10 ms ± 0.05 ms. Stable low thresholds were maintained for up to 6 years without significant variation from implant. Mean ventricular pulse width thresholds (0.12 ms ± 0.05 ms) were significantly higher (P < 0.001) than atrial thresholds (0.06 ms ± 0.03 ms) at implant and throughout the study period. The thresholds in the patients following cardiac surgery were comparable to those without previous cardiac surgery (P = NS). Stable low thresholds may be chronically maintatined for up to 6 years for epicardial steroid-eluting electrodes irrespective of pacing site or associated cardiac surgery.     

Chronic Performance of a Transvenous Steroid Pacing Lead Used as an Epi-Intramyocardial Electrode

Excessive surface fibrosis or fat limits effective electrode insertion in patients requiring epicardial pacing. We present chronic performance of a modified transvenous steroid lead used as an epi-intramyocardial electrode in a patient following repair of a univentricular heart after failure of both standard and steroid-eluting epicardial leads. Low implant threshold values remained stable during a 3-year postimplant interval demonstrating an effective and innovative approach to epicardial pacing.     

The Use of Active Fixation Electrodes for Permanent Endocardial Pacing Via a Persistent Left Superior Vena Cava

Two patients underwent permanent endocardial pacing for complete atrioventricular block. In each case a persistent left superior vena cava was either suspected or known to be present. An active fixation electrode was passed down the left superior vena cava and the tip positioned in the apex of the right ventricle. Stable ventricular pacing was achieved for the follow-up period of approximately six months. With the availability of such active fixation electrodes the presence of a persistent left superior vena cava no longer mandates insertion of an endocardial electrode via the right superior vena cava. when present, or implantation of an epicardial pacing system. (PACE, Vol. 5, March-April, 1982)     

"In-Line" Bipolar, Steroid-Eluting, High Impedance, Epimyocardial Pacing Lead

Recent advances in electrode surface designs have eliminated traditional threshold differences between endo- and epicardial pacing leads. Since the epicardial approach offers the potential of direct left ventricular pacing and the transvenous approach may not be feasible or warranted in all instances, more advanced leads are being designed to optimize epicardial pacing capabilities. This study was conducted to evaluate a bipolar epimyocardial lead. Six immature canines (age 3 months) were instrumented. The lead (Medtronic mode! 10389) is a single-pass, "in-line" bipolar electrode with low current drain and high impedance, with an intramyocardial steroid-eluting cathode and nonsteroid epicardial anode. Twelve ventricular leads were implanted (two per animal) and the animals followed for 6 months with weekly analysis of pacing and sensing capabilities. Results at explant were compared with implant values and showed no significant differences between sensed R waves or in R wave slew rates in unipolar or bipolar modes. Explant lead impedances remained high in both modes: bipolar, 1658 ± 331; and unipolar, 1327 ± 308 Ω (P < 0.05). Chronic voltage (V) threshold at 0.5 ms showed no significant change from implant values during the study: unipolar, 0.3 ± 0.06 versus 1.0 ± 0.8; and bipolar, 0.4 ± 0.06 versus 1.6 ± 1.2. Histologic review showed negligible fibrous reaction at the electrode-tissue interface. This study introduces a high impedance, low threshold, "in-line" bipolar pacing lead design capable of stable chronic pacing with implant facilitated by a single suture technique.     

Is Epicardial Dual Chamber Pacing a Realistic Alternative to Endocardial DDD Pacing? Initial Results of a Prospective Study

Seventeen patients, in whom an epicardial (n = 7) or a transvenous DDDM pacemaker system had been implanted between June 1988 and October 1990, were followed up for pacemaker and lead related complications, pacemaker longevity, and electrophysiological lead parameters. The mean follow-up interval was 18 +/- 12 months, maximum 34 months. There were no differences in chronic atrial and ventricular sensing thresholds between epicardial and endocardial stimulation, nor were there any differences concerning lead related complications between the two pacing modalities. However, atrial as well as ventricular chronic stimulation thresholds were significantly higher with epicardial stimulation resulting in a twofold increase in atrial energy consumption and a threefold increase in the ventricular energy consumption. Thus, in one patient with an epicardial DDD system, the pacemaker had to be replaced prematurely because of battery depletion. It is concluded that epicardial DDD stimulation can be reliably performed as far as atrial and ventricular sensing is concerned, but that the energy requirements of available myocardial leads are not satisfactory for making optimal use of modern pacemaker capability.